Therapeutic Intervention against Mitochondria Mediated Inflammation and Its Related Chronic Disorders

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: closed (31 March 2024) | Viewed by 1924

Special Issue Editors


E-Mail Website
Guest Editor
Department of Pharmaceutical Sciences, School of Pharmacy, University of Maryland Eastern Shore, Princess Anne, MD, USA
Interests: mitochondria; inflammation; chronic disease; cancer metastasis; neurodegenerative disease; apoptosis; ion channel modulation
Special Issues, Collections and Topics in MDPI journals
Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia
Interests: cancer metastasis; oxidative stress; inflammation; antioxidants

E-Mail Website
Guest Editor
Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia
Interests: cardiovascular diseases (ischemic heart diseases); ischemia reperfusion (IR) injury; inflammatory response; mechanisms of cardiotoxicity induced by different anti-cancer drugs

Special Issue Information

Dear Colleagues,

Mitochondria have recently developed as a key organelle and regulate cellular functions including cell proliferation or differentiation, cell death, metabolism, and cellular signaling, considered for inflammation-mediated diseases. Mitochondrial-evolved ROS has been implicated as a mediator for redox signaling, thereby causing stimulation of inflammatory proteins followed by mitochondrial deterioration and oxidative stress. Due to this kind of oxidative damage, chronic inflammation is believed to provoke several chronic diseases, including cancer and neurodegenerative disorders. In recent years, a promising insight into mitochondria-mediated cell death and inflammation has shed light on the molecular signature of the signaling machinery that could mediate different cascades of cell death and multiple kinds of inflammatory responses in chronic disease. Impairment of mitochondria-mediated anti-inflammatory machinery could cause an aggregation of unhealthy cellular components, followed by mitochondria-mediated cell death and its related episodes. To eradicate such cellular issues, and to explore whether novel strategies may be challenging therapeutic interventions, enriched delivery of the drugs and/or molecules to the impaired cells of patients with mitochondria-mediated chronic disorder is warranted. This Special Issue of Biomedicines aims to collect the original research articles and comprehensive reviews considering probable significance or impacts of pharmacotherapeutics on mitochondria-mediated inflammation and its mediated disease resistance in scientific community and healthcare settings.

Dr. Mohammad Waseem
Dr. Nemat Ali
Dr. Abdullah F. AlAsmari
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • mitochondrial dysfunction
  • inflammatory response
  • chronic disorder
  • cell death
  • novel drugs
  • pharmacological intervention
  • cancer
  • neurodegenerative disorder

Published Papers (2 papers)

Order results
Result details
Select all
Export citation of selected articles as:

Research

Jump to: Review

16 pages, 3410 KiB  
Article
Preventive Action of Beta-Carotene against the Indoxyl Sulfate-Induced Renal Dysfunction in Male Adult Zebrafish via Regulations of Mitochondrial Inflammatory and β-Carotene Oxygenase-2 Actions
by Arunachalam Muthuraman, Abu Sadat Md. Sayem, Sakthiganapathi Meenakshisundaram, Nemat Ali, Sheikh F. Ahmad, Abdullah F. AlAsmari, Shamama Nishat, Khian Giap Lim and Yamunna Paramaswaran
Biomedicines 2023, 11(10), 2654; https://doi.org/10.3390/biomedicines11102654 - 27 Sep 2023
Viewed by 1027
Abstract
Indoxyl sulfate (IS) is a metabolic byproduct of indole metabolism. IS readily interacts with the mitochondrial redox metabolism, leading to altered renal function. The β-carotene oxygenase-2 (BCO2) enzyme converts carotenoids to intermediate products. However, the role of β-carotene (BC) in IS-induced renal dysfunction [...] Read more.
Indoxyl sulfate (IS) is a metabolic byproduct of indole metabolism. IS readily interacts with the mitochondrial redox metabolism, leading to altered renal function. The β-carotene oxygenase-2 (BCO2) enzyme converts carotenoids to intermediate products. However, the role of β-carotene (BC) in IS-induced renal dysfunction in zebrafish and their modulatory action on BCO2 and mitochondrial inflammations have not been explored yet. Hence, the present study is designed to investigate the role of BC in the attenuation of IS-induced renal dysfunction via regulations of mitochondrial redox balance by BCO2 actions. Renal dysfunction was induced by exposure to IS (10 mg/L/hour/day) for 4 weeks. BC (50 and 100 mg/L/hour/day) and coenzyme Q10 (CoQ10; 20 mg/L/hour/day) were added before IS exposure. BC attenuated the IS-induced increase in blood urea nitrogen (BUN) and creatinine concentrations, adenosine triphosphate (ATP), and complex I activity levels, and the reduction of renal mitochondrial biomarkers, i.e., BCO2, superoxide dismutase-2 (SOD2), glutathione peroxidase-1 (GPX1), reduced and oxidized glutathione (GSH/GSSG) ratio, and carbonylated proteins. Moreover, renal histopathological changes were analyzed by the eosin and hematoxylin staining method. As a result, the administration of BC attenuated the IS-induced renal damage via the regulation of mitochondrial function. Full article
Show Figures

Figure 1

Review

Jump to: Research

12 pages, 245 KiB  
Review
Mitochondrial Dysfunction in Chronic Obstructive Pulmonary Disease: Unraveling the Molecular Nexus
by Chin-Ling Li, Jui-Fang Liu and Shih-Feng Liu
Biomedicines 2024, 12(4), 814; https://doi.org/10.3390/biomedicines12040814 - 07 Apr 2024
Viewed by 307
Abstract
Chronic obstructive pulmonary disease (COPD) is a prevalent and debilitating respiratory disorder characterized by persistent airflow limitation and chronic inflammation. In recent years, the role of mitochondrial dysfunction in COPD pathogenesis has emerged as a focal point of investigation. This review endeavors to [...] Read more.
Chronic obstructive pulmonary disease (COPD) is a prevalent and debilitating respiratory disorder characterized by persistent airflow limitation and chronic inflammation. In recent years, the role of mitochondrial dysfunction in COPD pathogenesis has emerged as a focal point of investigation. This review endeavors to unravel the molecular nexus between mitochondrial dysfunction and COPD, delving into the intricate interplay of oxidative stress, bioenergetic impairment, mitochondrial genetics, and downstream cellular consequences. Oxidative stress, a consequence of mitochondrial dysfunction, is explored as a driving force behind inflammation, exacerbating the intricate cascade of events leading to COPD progression. Bioenergetic impairment sheds light on the systemic consequences of mitochondrial dysfunction, impacting cellular functions and contributing to the overall energy imbalance observed in COPD patients. This review navigates through the genetic landscape, elucidating the role of mitochondrial DNA mutations, variations, and haplogroups in COPD susceptibility and severity. Cellular consequences, including apoptosis, autophagy, and cellular senescence, are examined, providing insights into the intricate mechanisms by which mitochondrial dysfunction influences COPD pathology. Therapeutic implications, spanning antioxidant strategies, mitochondria-targeted compounds, and lifestyle modifications, are discussed in the context of translational research. Important future directions include identifying novel biomarkers, advancing mitochondria-targeted therapies, and embracing patient-centric approaches to redefine COPD management. This abstract provides a comprehensive overview of our review, offering a roadmap for understanding and addressing the molecular nexus between mitochondrial dysfunction and COPD, with potential implications for precision medicine and improved patient outcomes. Full article
Back to TopTop